As a Cancer Develops the Mutation Rate Accelerates

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The Answer is The average rate of mutation in human cells is low (about 10^-6per gene per cell) and the majority of cancer-causing mutations are recessive at the cellular level, so that both alleles need to be mutated. Cancer might therefore be expected to be highly improbable: the chance that any cell would receive successive mutations, often in both alleles, at several cancer-susceptibility loci would normally be vanishingly small. Cancer nevertheless is common, and altered expression at a few cancer- susceptibility loci can be sufficient. One major explanation is that early driver mutations greatly increase the probability of later mutations in two ways, as listed below.
1) The first way is by giving the cell a growth advantage. If cells with a driver mutation have an increased growth rate, they will produce more progeny than other cells and will produce an expanded target of mutant cells, thereby increasing the probability of a subsequent mutation (see Figure 10.4A).
2) The second, and most important, way of increasing the probability of later mutations in cancer is by destabilizing the genome. Chromosome instability is a feature of most tumor cells, producing grossly abnormal karyotypes with abnormal numbers of chromosomes and frequent structural arrangements that can activate oncogenes or cause a loss of tumor suppressor genes. In some cancers, a form of global DNA instability occurs-it is caused by mutations in key DNA repair genes and can result in greatly elevated mutation rates. Mutations in genes that regulate epigenetic modifications result in additional epigenetic instability that can result in altered expression at cancer-susceptibility loci. Additionally, some types of epigenetic change cause genome instability.

As a Cancer Develops the Mutation Rate Accelerates

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As a Cancer Develops the Mutation Rate Accelerates

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